Studies have continued on selected aspects of the mechanism of biochemical activation of cells involved in immunologic inflammation, including mast cells, basophils, lymphocytes, and phagocytic cells. Areas receiving major emphasis have included: 1) the structure, biosynthesis, heterogeneity, and degradation of slow reacting substance in human and rat basophilic leukemia cells, rat mast cells, and antigen-stimulated guinea pig lung; 2) the chemical nature, heterogeneity, biosynthesis, and basis for functional activity of the IgE receptor on human and rat basophilic leukemia cells; 3) early activation events in lectin-stimulated human lymphocytes, particularly from the point of view of new cell surface macromolecules that are synthesized, changes in protein phosphorylation, and differences between lectins in terms of how they affect intracellular metabolism; 4) the role of lipoxygenase products such as 5- and 12-hydroxy-eicosatetraenoic acids, 5,12-di-hydroxy-eicosatetraenoic acid, and cyclic nucleotides in lysosomal enzyme release, intracellular oxidation, and amino acid and calcium transport in lymphocytes and polymorphonuclear leukocytes with particular emphasis on the possible role of esterification of the hydroxylated fatty acids into membrane phospholipids and triglycerides as a basis for their action; 5) investigation of the role of cellular immunity and alterations in lymphocyte subpopulations in forms of inflammatory bowel disease; 6) efforts to develop monoclonal and other antisera to human T lymphocyte antigens with the goal of improving the subclassification of T lymphocytes; 7) the development of better reagents to study the complement component, C3d, and to further evaluate the role of complement in human disease.